ライフサイエンスコーパス: oxygen free radical

1 of MCP-1 may be stimulated by cytokines and oxygen free radicals.

2 philic response, which causes the release of oxygen free radicals.

3 nt in tumor tissue prevents the formation of oxygen free radicals.

4 are mediated via the formation of NE-derived oxygen free radicals.

5 cytochrome oxidase, and (5) the formation of oxygen free radicals.

6 Both STGP and LTGP gels produced oxygen free radicals.

7 , at least in part through the generation of oxygen free radicals.

8 nhance phagocytic activity and generation of oxygen free radicals.

9 ave been proposed as a significant source of oxygen free radicals.

10 n thiols and inhibits cellular damage due to oxygen free radicals.

11 disorders linked to excessive generation of oxygen free radicals.

12 are related to its role in the generation of oxygen free radicals.

13 s in PD involves the accumulation of harmful oxygen free radicals.

14 stnatal exposure to environmental sources of oxygen free radicals.

15 tients may be related to oxidative damage by oxygen free radicals.

16 smutases (SODs) protect cells from damage by oxygen free radicals.

17 and which are formed in DNA by the action of oxygen-free radicals.

18 rophils by contact, leading to production of oxygen free radicals accompanied by release of granule p

19 (2) Oxygen free radicals also appear to mediate the hypoxic-

20 The UVA-dependent generation of oxygen free radicals also oxidized ASA at a 10(3) faster

21 y to alloxan, a generator of highly reactive oxygen free radicals and a potent beta-cell toxin.

22 ve stress; increased protein modification by oxygen free radicals and an elevated concentration of th

23 Because NFkappaB is a target of oxygen free radicals and Bcl-2 is an antioxidant gene, w

24 This injury is attributed in part to oxygen free radicals and has been partially ameliorated

25 ic newborn piglets through the generation of oxygen free radicals and induction of lipid peroxidation

26 Exercise increases the generation of oxygen free radicals and lipid peroxidation.

27 as previously believed to be accomplished by oxygen free radicals and other reactive oxygen species g

28 n-superoxide dismutase (SOD1) would diminish oxygen free radicals and reduce alcohol-induced liver in

29 he affected tissues produce large amounts of oxygen-free radicals and NO.

30 such mucosal injury is initially mediated by oxygen free radicals, and because mitogen-activated prot

31 se is especially vulnerable to inhibition by oxygen free radicals, and the upstream metabolites, pyru

32 elated cytokines; b) increased production of oxygen free radicals associated with ischemia/reperfusio

33 MPP(+), unlike rotenone, did not produce oxygen free radicals, but rather blocked ATP production

34 Generation of oxygen free radicals by treatment of telencephalic mitoc

35 The production of oxygen free radicals catalysed by non-haem iron was inve

36 hypoxic-ischemic brain injury by generating oxygen-free radicals during reperfusion.

37 These results suggest that oxygen-free radicals, especially superoxide anions, are

38 ate that CECs produce significant amounts of oxygen free radicals following ischemia, primarily from

39 lity to sequester iron from participation in oxygen free radical formation is consistent with a cytop

40 Oxygen-free radicals formed during normal aerobic cellul

41 3'-blocking groups formed from the action of oxygen free radicals generated during normal cellular me

42 These results suggest that a burst of oxygen free radicals generated during the initial period

43 Oxygen free radicals, generated by cerebral ischemia, ha

44 se results directly demonstrate an increased oxygen free radical generation during hypoxia and sugges

45 The direct demonstration of oxygen free radical generation during hypoxia is the cri

46 The role of oxygen free radical generation during reversible focal c

47 the hypothesis that maternal hypoxia induces oxygen free radical generation in the fetal guinea pig b

48 ly decreased the hypoxia-induced increase in oxygen free radical generation in the term fetal guinea

49 reserved liver cells is not mediated by: (1) oxygen free radical generation or improved by antioxidan

50 Allantoin, a marker of oxygen free radical generation, decreased by 20% after a

51 f neutrophil phagocytosis and a reduction in oxygen free radical generation, which may contribute to

52 are deficient in myeloid cell activation and oxygen free radical generation.

53 TP metabolism are the primary candidates for oxygen free radical generation: (a) MPTP oxidation to MP

54 In order to promote oxygen-free radical generation, hypoxanthine (n=9) or xa

55 The involvement of oxygen free radicals has been suggested in c-fos activat

56 Oxygen free radicals have been implicated in beta-cell d

57 Elevated levels of oxygen free radicals have been implicated in the pathway

58 Oxygen free radicals have been invoked as mediators of t

59 Oxygen free radicals have been proposed to mediate amylo

60 Superoxide anion and other oxygen-free radicals have been implicated in the pathoge

61 These results not only support a role for oxygen free radicals in beta-AP toxicity but also highli

62 data, for the first time, suggest a role of oxygen free radicals in causing abnormality of female re

63 These data support a role of oxygen free radicals in promoting post-anoxic mitochondr

64 e, from the production and detoxification of oxygen free radicals in the mitochondrion to the efficac

65 f the Bad pathway after tFCI and the role of oxygen free radicals in the regulation of apoptosis rema

66 ): Each does indeed bind copper and scavenge oxygen-free radicals in vivo.

67 e hypoxia results in increased generation of oxygen-free radicals including nitric oxide (NO), expres

68 Anticancer modalities based on oxygen free radicals, including photodynamic therapy and

69 We tested the hypothesis that oxygen free radicals induce an increase in ODC activity

70 ly of UV radiation-induced, but also of some oxygen free radical-induced, DNA lesions.

71 ment of S phase cells with agents that cause oxygen free radicals induces the dephosphorylation of DN

72 physiologic outcome following treatment with oxygen free radical inhibitors and scavengers.

73 cally accompanied by increased production of oxygen free radicals, is a cause and a consequence of ce

74 ogue 21 which were effective in reducing the oxygen free radical level.

75 ated metabolic changes leading to changes in oxygen free radical levels, which in turn lead to the in

76 hat in tumor cells, endogenous production of oxygen free radicals may be a major factor in promoting

77 nhanced muscle fatigue, whereas formation of oxygen free radicals may be attenuated by endogenous pro

78 Oxygen free radicals may play a pivotal role in the mito

79 asic pattern consisting of both acute phase (oxygen free radical mediated) and subacute phase (neutro

80 d to damage dopamine-secreting neurons by an oxygen free radical-mediated mechanism.

81 Thus, reductions in oxygen free radical-mediated vascular injury may contrib

82 in piglets have shown that the generation of oxygen free radicals (O(-)(2)) following traumatic brain

83 The generation of oxygen free radicals (OFR) and tissue infiltration by ac

84 t hypoxia induces an increased production of oxygen free radicals (OFR) in the brain of the guinea pi

85 Oxygen free radicals (OFRs) have been implicated in the

86 Oxygen free radicals oxidize arachidonic acid to a compl

87 (1) Oxygen free radicals, particularly hydroxyl radical (OH.

88 However, the role of oxygen free radicals produced after ischemia/reperfusion

89 anistically, spermine neutralized off-target oxygen free radicals produced by NADPH oxidase-1 (Nox1)(

90 Oxygen free radical production also increased MCP-1 mRNA

91 ) isolated from piglet cortex to measure CEC oxygen free radical production and determine its role in

92 n is increased xanthine oxidase (XO)-derived oxygen free radical production and endothelial dysfuncti

93 tion in nNOS-/- mice may relate to decreased oxygen free radical production and related NO reaction p

94 plug capillary-sized pores and show enhanced oxygen free radical production may account for the exces

95 -/-) embryonic fibroblasts demonstrated high oxygen free radical production when exposed to hemin, hy

96 Blockade of oxygen free radical production with superoxide dismutase

97 inergic PC12 cell cultures, does not involve oxygen free radical production, but rather may be caused

98 n were increased in response to cytokines or oxygen free radical production, but the magnitude and du

99 A 55% increase in oxygen free radical production, determined by fluorescen

100 f energy metabolism, oxygen consumption, and oxygen free radical production, it becomes imperative to

101 (NO radical) exhibit changes in the rate of oxygen free radical production.

102 Targeting uremic toxins, oxygen-free radical production and the mitophagy process

103 ive phosphorylation were also decreased, and oxygen-free radical production increased.

104 Variable factors, including accumulation of oxygen free radicals, protein conformational changes, de

105 Short-lived oxygen free radicals react with the spin trap and produc

106 d coronary endothelial dysfunction caused by oxygen free radicals released during reperfusion.

107 (+)/H(+) exchange blocker (amiloride), or an oxygen free radical scavenger (vitamin E).

108 treatment with N-acetyl-l-cysteine (NAC), an oxygen free radical scavenger, led to a reduction in the

109 Significantly, treatment with an oxygen free radical scavenger, N-acetyl-l-cysteine (NAC)

110 se results support the concept of developing oxygen free radical scavengers for both AD and PD and fu

111 ve stability and high generation of reactive oxygen free radical species.

112 ectron oxidation of hydrogen peroxide to the oxygen free radical, superoxide.

113 ble of generating significantly greater ROS (oxygen free radicals) than nondiabetic blood (P < 0.05).

114 ine and xanthine, xanthine oxidase generates oxygen free radicals that cause postischemic injury.

115 es are associated with the overproduction of oxygen free radicals that inflict cell damage.

116 We examined the role of XO in generating oxygen-free radicals that cause brain injury, hypothesiz

117 t the idea that MPTP toxicity is mediated by oxygen free radicals, we assessed lipid peroxidation and

118 Activation and oxygen free radicals were assessed using gp91(phox-/-) m

119 Oxygen free radicals were measured by ESR spectroscopy i

120 pathophysiologic production of cytokines and oxygen free radicals, which potentiate organ injury in s